Effects of pituitary adenylate cyclase activating polypeptide (PACAP) and vasoactive intestinal polypeptide (VIP) on the cardiovascular system in sheep

Sawangjaroen, Kitja; Dallemagne, Catherine; Cross, R. B.; Curlewis, J. D.

doi:10.1016/0196-9781(92)90068-e

Cited by 29 publications

(7 citation statements)

References 12 publications

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“…Heart rate returned to normal within 5 min after the infusion had been discontinued. The cardiovascular effects of infusion of PACAP or VIP in conscious sheep at the full range of doses used in this experiment have been reported elsewhere in more detail (26). PACAP also had suppressive effects on G H secretion ( Fig.…”

Section: E-xperinwnt 1: Intracarotid Infusion Of Pa C a P And Vipmentioning

confidence: 85%

Effects of Pituitary Adenylate Cyclase‐Activating Polypeptide (PACAP) and Vasoactive Intestinal Polypeptide (VIP) on Prolactin, Luteinizing Hormone and Growth Hormone Secretion in the Ewe

Sawangjaroen

Curlewis

1994

J Neuroendocrinology

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This study was undertaken to investigate the roles of PACAP and VIP in the control of pituitary hormone secretion in the ewe. The first experiment was designed to identify any direct effects at the level of the pituitary and was conducted during the luteal phase of a prostaglandin-synchronized oestrous cycle. PACAP (0.008, 0.04, 0.2 and 1.0 nmol/min) or VIP (0.06, 0.2, 0.6 and 1.8 nmol/min) was infused into the carotid artery over a 10 min period. Blood samples were taken before and after the infusions so that plasma PRL, LH and GH concentrations could be measured. Blood pressure was also monitored to determine if the doses used were biologically active. In no case was an effect on hormone secretion observed. In contrast, the highest dose of each peptide induced an increase in heart rate to almost three-fold the resting value. Although both peptides are active in vivo, this result suggests that neither peptide has a direct effect on hormone release from the pituitary of prostaglandin-synchronized ewes. In a second experiment, we investigated whether the peptides had central effects on hormone secretion. Intracerebroventricular (ICV) injection of PACAP or VIP at the dose 10 nmol was tested in ovariectomized ewes. After injection, PACAP suppressed PRL and GH secretion so that plasma hormone concentrations from 1-3 h after injection were significantly different from the control (P < 0.05 for PRL, P < 0.01 for GH). In addition, PACAP significantly reduced mean LH concentration (P < 0.05) and LH pulse frequency (P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: E-xperinwnt 1: Intracarotid Infusion Of Pa C a P And Vipmentioning

confidence: 85%

Effects of Pituitary Adenylate Cyclase‐Activating Polypeptide (PACAP) and Vasoactive Intestinal Polypeptide (VIP) on Prolactin, Luteinizing Hormone and Growth Hormone Secretion in the Ewe

Sawangjaroen

Curlewis

1994

J Neuroendocrinology

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“…Using the same experimental model, Will-Shahab and coworkers (1993) detected a long-lasting positive chronotropic effect by application of 10 nM PACAP(1-38). In sheep, PACAP and VIP induced an increase in heart rate while the mean arterial blood pressure decreased (Sawangjaroen et al 1992). In contrast, PACAP induced severe bradycardia after transient tachycardia in anesthetized beagle dogs (Ishizuka et al 1992).…”

Section: Discussionmentioning

confidence: 99%

PACAP induces bradycardia in guinea-pig heart by stimulation of atrial cholinergic neurones

Seebeck

Schmidt

Kilbinger³

et al. 1996

Naunyn-Schmiedeberg's Arch Pharmacol

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Based on previous studies which indicated that pituitary adenylate cyclase activating peptide (PACAP) acts as a positive inotropic and chronotropic substance in different species via the cAMP signal transduction pathway, the objective of the present work was to investigate cAMP-regulated myocardial key proteins in response to PACAP in isolated ventricular cells of the guinea pig. Surprisingly, the two molecular forms of PACAP, PACAP(1-27) and PACAP(1-38), showed no effect on intracellular cAMP-levels, L-type Ca2+ channel current or phosphorylation of troponin inhibitor (TnI) and phospholamban (PLB). Additionally, inotropy of isolated guinea-pig ventricular strips was not affected by the neuropeptide. However, in isolated spontaneously beating guinea-pig atria, PACAP(1-27) and PACAP(1-38), but not VIP induced severe bradycardia in a dose-dependent manner. This effect could be prevented by preincubation with the PACAP receptor antagonist PACAP(6-38), by atropine and by omega-conotoxin, a blocker of neuronal N-type Ca2+ channels. PACAP stimulates release of [3H]-labelled acetylcholine. Only preparations showing an increase in [3H]acetylcholine release developed bradycardia, indicating a causal relationship between both phenomena. It was concluded that PACAP exerts no influence on guinea-pig ventricular tissue, but induces negative chronotropic effects in isolated guinea-pig atria by stimulation of acetylcholine release from parasympathetic neurons via PACAP type 1 receptors.

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“…This remarkable ability of PACAP to diffuse through the BBB is a great asset for the development of a treatment and likely accounts for the neuroprotective effects of PACAP observed in vivo after intravenous injection. Nevertheless, PACAP or metabolically stable analogs can interact with PAC1, VPAC1, and VPAC2 receptors to induce peripheral side effects, notably on the cardiovascular system where PACAP would induce vasodilatation and increase heart rate (Nandha et al 1991;Sawangjaroen et al 1992). Taking into account that the PAC1 receptor mediates most of the antiapoptotic effects of PACAP, it would be interesting to develop a specific PAC1 receptor agonist.…”

Section: Perspectives-pacap As a Pharmacological Tool Against Neuronamentioning

confidence: 98%

Inhibitory Effect of PACAP on Caspase Activity in Neuronal Apoptosis: A Better Understanding Towards Therapeutic Applications in Neurodegenerative Diseases

et al. 2008

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Programmed cell death, which is part of the normal development of the central nervous system, is also implicated in various neurodegenerative disorders. Cysteine-dependent aspartate-specific proteases (caspases) play a pivotal role in the cascade of events leading to apoptosis. Many factors that inhibit cell death have now been identified, but the underlying mechanisms are not fully understood. Pituitary adenylate cyclase-activating polypeptide (PACAP) has been shown to exert neurotrophic activities during development and to prevent neuronal apoptosis induced by various insults such as ischemia. Most of the neuroprotective effects of PACAP are mediated through the PAC1 receptor. This receptor activates a transduction cascade of second messengers to stimulate Bcl-2 expression, which inhibits cytochrome c release and blocks the activation of caspases. The inhibitory effect of PACAP on the apoptotic cascade suggests that selective, stable, and potent PACAP derivatives could potentially be of therapeutic value for the treatment of post-traumatic and/or chronic neurodegenerative processes.

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Effects of pituitary adenylate cyclase activating polypeptide (PACAP) and vasoactive intestinal polypeptide (VIP) on the cardiovascular system in sheep

Cited by 29 publications

References 12 publications

Effects of Pituitary Adenylate Cyclase‐Activating Polypeptide (PACAP) and Vasoactive Intestinal Polypeptide (VIP) on Prolactin, Luteinizing Hormone and Growth Hormone Secretion in the Ewe

Effects of Pituitary Adenylate Cyclase‐Activating Polypeptide (PACAP) and Vasoactive Intestinal Polypeptide (VIP) on Prolactin, Luteinizing Hormone and Growth Hormone Secretion in the Ewe

PACAP induces bradycardia in guinea-pig heart by stimulation of atrial cholinergic neurones

Inhibitory Effect of PACAP on Caspase Activity in Neuronal Apoptosis: A Better Understanding Towards Therapeutic Applications in Neurodegenerative Diseases

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